What is the purpose of music? A review of evolutionary and pleasurable research findings

Ever wonder what happens in your brain and body when you get chills from a musical performance?

This 2013 summary review of 126 studies provided details of brain areas that contribute to our enjoyment of music.

Much of the review addressed Darwin’s observation that music had no readily apparent functional consequence and no clear-cut adaptive function. The researchers noted that:

“There is scant evidence that other species possess the mental machinery to decode music in the way humans do, or to derive enjoyment from it.”


The reasons why different types of music affect us differently are similar to the findings of the Reciprocity behaviors differ as to whether we seek cerebral vs. limbic system rewards study.

Here are the “We seek limbic system rewards” similarities:

“The nucleus accumbens played an important role with both familiar and novel music. In the case of familiar music, hemodynamic activity in the nucleus accumbens was associated with increasing pleasure, and maximally expressed during the experience of chills, which represent the peak emotional response; these were the same regions that showed dopamine release. The nucleus accumbens is tightly connected with subcortical limbic areas of the brain, implicated in processing, detecting, and expressing emotions, including the amygdala and hippocampus. It is also connected to the hypothalamus, insula, and anterior cingulate cortex, all of which are implicated in controlling the autonomic nervous system, and may be responsible for the psychophysiological phenomena associated with listening to music and emotional arousal.”

Here is the “We seek cerebral rewards” part.

“Finally, the nucleus accumbens is tightly integrated with cortical areas implicated in “high-level” processing of emotions that integrate information from various sources, including the orbital and ventromedial frontal lobe. These areas are largely implicated in assigning and maintaining reward value to stimuli and may be critical in evaluating the significance of abstract stimuli that we consider pleasurable.”

http://www.pnas.org/content/110/Supplement_2/10430.full “From perception to pleasure: Music and its neural substrates”

Using expectations of oxytocin to induce positive placebo effects of touching

This 2013 Scandinavian study detailed which brain structures were involved when fooling oneself about actual sensations in favor of expected sensations.

It was hilarious how the researchers used studies of oxytocin to create expectations in the subjects:

“To induce expectation of intranasal oxytocin’s beneficial effects on painful and pleasant touch experience, participants viewed a 6-min locally developed video documentary about oxytocin’s putative prosocial effects such as involvement in bonding, love, grooming, affective touch, and healing. As all of the material was based on published research, there was no deception. The video concluded that a nasal spray of oxytocin might enhance the pleasantness of:

  • (i) stroking and
  • (ii) warm touch, and
  • (iii) reduce the unpleasantness of pain.”

Other items:

  • Only the placebo effects for the warm and pain-reducing touches were statistically significant, not the stroking touch;
  • The a priori brain areas monitored in the “sensory circuitry” included the thalamus and were all in the right brain hemisphere;
  • The a priori brain areas monitored in the “emotional appraisal circuitry” included the amygdala.

One way the researchers summarized the study was:

“Pain reduction dampened sensory processing in the brain, whereas increased touch pleasantness increased sensory processing.”

This finding demonstrated how the thalamus part of the limbic system actively controls and gates information to and from the cerebrum, similar to the Thalamus gating and control of the limbic system and cerebrum is a form of memory study.


There was a terminology problem in the study, evidenced by statements such as:

“We induced placebo improvement of both negative and positive feelings (painful and pleasant touch).”

Touch is a sensation, not a feeling or emotion. This placebo study created expectations of sensations in the subjects’ cerebrums, not expectations of emotions.

Also, including parts of the limbic system such as the amygdala in the “emotional appraisal circuitry” didn’t mean that the researchers studied feelings or emotions. We know from research summarized in the Conscious mental states should not be the first-choice explanation of behavior study that:

“Neither amygdala activity nor amygdala-controlled responses are telltale signatures of fearful feelings.

The current study cast additional light on the dubious Problematic research on human happiness study. Those researchers were fooled by a positive placebo effect!

http://www.pnas.org/content/110/44/17993.full “Placebo improves pleasure and pain through opposite modulation of sensory processing”

What happens next after a detox program predictably fails?

This 2014 study was a misguided example of looking solely at the presenting parts of a person’s condition rather than the whole historical person.

What did this study’s researchers decide after finding:

“Alcohol-dependent subjects..remained with high scores of depression, anxiety, and alcohol craving after a short-term detoxification program.”

Was it that the detox program didn’t work because it dealt with suppressing symptoms rather than addressing causes?

NO!

The researchers decided:

“Gut microbiota seems to be a previously unidentified target in the management of alcohol dependence.”

The researchers proceeded on some trendy, in-vogue aspect of their patients with which to tinker.

The researchers ignored that the correlation of the new treatment course didn’t show causation. They also ignored underlying causes for the ineffectiveness of the preceding treatments of symptoms.

Hard to see how the reviewer believed that this study would advance science.

Meanwhile, the researchers continued to ignore the elephants in the room: the relationships of the patients’ histories and their pain.

http://www.pnas.org/content/111/42/E4485.full “Intestinal permeability, gut-bacterial dysbiosis, and behavioral markers of alcohol-dependence severity”

If research provides evidence for the causes of stress-related disorders, why only focus on treating the symptoms?

This 2014 rodent research reliably induced many disorders common to humans. Here are some post-birth problems the researchers caused, primarily by applying different types of stress, as detailed in the study’s supplementary material:

Yet the researchers’ goal was to identify a brain receptor for:

“Novel therapeutic targets for stress-related disorders.”

In other words, develop new drugs to treat the symptoms.


Where are the studies that have goals to prevent these common problems being caused in humans by humans?

Where is the research on treatments to reverse the enduring physiological impacts to stress by treating the causes?


What do you think of this excerpt?

“Accumulating evidence suggests that traumatic events particularly during early life (e.g., parental loss or neglect) coupled with genetic factors are important risk factors for the development of depression and anxiety disorders.

Moreover, the brain is particularly vulnerable to the effects of stress during this period.

Maternal separation in rodents is a useful model of early-life stress that results in enduring physiological and behavioral changes that persist into adulthood, including increased hypothalamic–pituitary–adrenal (HPA)–axis sensitivity, increased anxiety, and visceral hypersensitivity.”

http://www.pnas.org/content/111/42/15232.fullGABAB(1) receptor subunit isoforms differentially regulate stress resilience”

How to make a child less capable even before they are born: stress the pregnant mother-to-be

This 2014 rodent study showed how to make a less-capable pup by stressing the mother early in gestation. The study centered on a placental enzyme (OGT) that translates a mother’s stress into neuroprogramming of her developing fetus.

One finding was that this enzyme was less plentiful when the fetus was male compared with female.

Another finding was that the enzyme was less plentiful when the mother was stressed early in gestation, compared with unstressed mothers.

Informed by the first two findings, the researchers studied the placentae of male pups where the mother was stressed early in gestation. They found that these placentae had lower levels of an enzyme (Hsd17b3) that converts the precursor androstenedione into testosterone.

The resultant finding was that the male pups of stressed mothers had lower levels of testosterone than the control group of male pups.

A fourth finding was that offspring of both sexes born with a placenta where the OGT enzyme was less plentiful had 10-20% less body weight, a condition that developed after weaning. The researchers attributed this finding to reduced mitochondrial function in the hypothalamus compared with normal mice.

http://www.pnas.org/content/111/26/9639.full “Targeted placental deletion of OGT recapitulates the prenatal stress phenotype including hypothalamic mitochondrial dysfunction”

Are stress-induced epigenetic changes to DNA inherited across generations?

This 2014 Geneva/Cambridge plant study ended by stating:

“The unequivocal demonstration of transgenerational transmission of environmentally-induced epigenetic traits remains a significant challenge.

One of the critical activities erasing stress memories is conserved between plants and mammals.”

However, the researchers didn’t demonstrate that their findings were broadly applicable for mammals or organisms other than the specific plant variety they studied. Possible reasons for these limited findings were given in a 2015 Australian study referenced by Mechanisms of stress memories in plants:

“The majority of DNA methylation analyses performed in plants to date have focused on Arabidopsis, despite being relatively depleted of TEs [transposable elements] (15–20% of the genome) and being poorly methylated compared to other plant genomes.

These studies have lacked the resolution to provide the specific context and genomic location of the changes in DNA methylation.”

There are also significant differences in how epigenetic inheritance across generations may operate among different species per Epigenetic reprogramming in plant and animal development.


Neither the current study nor the above review addressed the behavioral aspect of stress-induced epigenetic inheritance across generations. For example, the behavior of a mother whose DNA was epigenetically changed by stress can induce the same epigenetic changes to her child’s DNA when her child is stressed per One way that mothers cause fear and emotional trauma in their infants:

“Our results provide clues to understanding transmission of specific fears across generations and its dependence upon maternal induction of pups’ stress response paired with the cue to induce amygdala-dependent learning plasticity.”

http://www.pnas.org/content/111/23/8547.full “Identification of genes preventing transgenerational transmission of stress-induced epigenetic states”

DNA methylation is the most frequent way that duplicate genes are epigenetically silenced

This 2014 human study showed that DNA methylation was the most frequent way that duplicate genes were epigenetically silenced. Current thinking is that at least half of the genes in the human genome are inactive duplicates.

The study stated:

“Duplicate genes are essential and ongoing sources of genetic material.”

What the researchers didn’t show, however, was that duplicate genes evolve per the study’s title “evolution of duplicate genes.” It was misleading to imply in the study’s headline that duplicate genes evolve.

Evolution occurs as organisms adapt to their environments. Duplicate genes aren’t active in the adaptation process when they are silenced.

http://www.pnas.org/content/111/16/5932.full “DNA methylation and evolution of duplicate genes”

Hypothalamic oxytocin and vasopressin have sex-specific effects on pair bonding, gregariousness, and aggression

This 2014 bird study showed the complementary effects of neurochemicals vasopressin and oxytocin in the hypothalamus.

Oxytocin neurons in the hypothalamus promote pair bonding and gregariousness in females.

Vasopressin neurons in the hypothalamus promote maternal care, social recognition, and gregariousness in both males and females, and aggression in males toward females.

Vasopressin and oxytocin released generally and in other parts of the brain have different effects. For example:

“Central administration of oxytocin also attenuates stress-induced effects on the brain and reverses stress-induced social avoidance.”

http://www.pnas.org/content/111/16/6069.full “Hypothalamic oxytocin and vasopressin neurons exert sex-specific effects on pair bonding, gregariousness, and aggression in finches”

Flooding the hypothalamus with neurochemicals affects reward-seeking, motivated, and depressive behavior

This 2014 rodent study showed the opposing effects of neurochemicals orexin (excitator) and dynorphin (inhibitor) in the hypothalamus.

The hypothalamus plays a role in behaviors such as addiction and impulsiveness. Food and cocaine self-administration were the main techniques used.

Flooding the hypothalamus with orexin produced reward-seeking and motivated behavior. That was greatly reduced when dynorphin levels were increased, and depressive behavior set in.

http://www.pnas.org/content/111/16/E1648.full “Hypocretin (orexin) facilitates reward by attenuating the antireward effects of its cotransmitter dynorphin in ventral tegmental area”

Do researchers have to be cruel to our fellow primates to adequately research oxytocin?

This 2014 primate study found:

“Oxytocin increased infants’ affiliative communicative gestures and decreased salivary cortisol, and higher oxytocin levels were associated with greater social interest.”

One would have to take an anti-evolutionist stance and believe that primates do not feel what humans feel to consider this process to NOT be cruel:

“To test these macaques, we took advantage of ongoing experiments requiring infants to be separated from their mother on the day of birth. Infants were nursery-reared, housed individually, with a cloth surrogate mother. They could see and hear other infants, but could not touch them.”

We know that primate infants, like humans, need nourishment, transportation, warmth, protection, and socialization from their mothers. What level of findings about oxytocin can a research study make that would justify this deprivation?

It surely wasn’t the findings this study made. We knew without doing the study that getting oxytocin from a nebulizer would be nowhere near an acceptable substitute for a mother’s touch and care.

http://www.pnas.org/content/111/19/6922.full “Inhaled oxytocin increases positive social behaviors in newborn macaques”

Problematic research on oxytocin: If the study design excludes women, its findings cannot include women

This 2014 study’s findings that “the hormone oxytocin promotes group-serving dishonesty” can’t apply generally to humans because its subjects were ALL men.

Regarding oxytocin, the researchers certainly knew or should have known previous studies’ findings about sex differences, as did Is oxytocin why more women than men like horror movies? which cited:

“Oxytocin modulates brain activity differently in male and female subjects.”

Regarding differing reciprocal behaviors, the researchers also knew or should have been better informed about associated brain areas through studies such as Reciprocity behaviors differ as to whether we seek cerebral vs. limbic system rewards and its references.

And how could the study produce reliable, replicable evidence of:

Dishonesty to be plastic and rooted in evolved neurobiological circuitries”

when the researchers performed NO measurements of “neurobiological circuitries” that supported that finding?

What was the agenda in play here? What did the female Princeton reviewer see in this study that advanced science?

http://www.pnas.org/content/111/15/5503.full “Oxytocin promotes group-serving dishonesty”


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Is oxytocin why more women than men like horror movies?

This 2014 human study showed how oxytocin regulates serotonin with the involvement of the right part of the amygdala.

The following passage caught my eye as a possible explanation of why more women than men prefer horror movies: oxytocin?

“We have chosen to enroll male subjects only to avoid the confounding effects linked to sex and a possible interaction with gonadal steroids. Indeed, as shown by previous studies, oxytocin modulates brain activity differently in male and female subjects.

For instance, oxytocin suppresses amygdala response to emotionally threatening stimuli in males but enhances the same response in females.

http://www.pnas.org/content/111/23/8637.full “Switching brain serotonin with oxytocin”

Who benefits when research with no practical application becomes a politically correct meme?

Do you take a risk, as this 2013 University of Texas/Yale study concluded, because you don’t foresee how you can avoid the risk?

By making this finding, the study essentially assigned the bases of a person’s risky decisions to their cerebrum.

I wasn’t persuaded. The conclusion was reached because the study’s design only engaged the subjects’ cerebrums with a video game task involving popping balloons. See Task performance and beliefs about task responses are solely cerebral exercises for a similar point.

If the researchers had instead designed a study that also engaged the subjects’ limbic system and lower brains, the findings may have been different.


Only one of the news articles covered this story with some accuracy, io9.com:

Helfinstein (the lead researcher) doesn’t see any direct, practical applications of the research. After all, people don’t spend their lives in fMRI scanners, so it’s not as if we can tell when people are going to make a risky decision in their day-to-day activities.”

Compare that with the majority of the news coverage that hijacked the study’s findings to try to develop a politically correct meme:

“Many health-relevant risky decisions share this same structure, such as when deciding how many alcoholic beverages to drink before driving home or how much one can experiment with drugs or cigarettes before developing an addiction.”

The study found that “risk taking may be due, in part, to a failure of the control systems necessary to initiate a safe choice.” The brain areas were “primarily located in regions more active when preparing to avoid a risk than when preparing to engage in one.” These areas included the “bilateral parietal and motor regions, anterior cingulate cortex, bilateral insula, and bilateral lateral orbitofrontal cortex.”

Notice that just one of the studied brain areas (the anterior cingulate cortex) is part of the limbic system or lower brains, although the bilateral insula connects to the limbic system. Yet the limbic system and lower parts of the brain are most often the brain areas that drive real-world risky behaviors such as smoking, drug use, sexual risk taking, and unsafe driving.

A video game task of popping balloons that engaged the cerebrum was NOT informative to the cause-and-effect of the emotions and instincts and impulses from limbic system and lower brains that predominantly drive risky behavior.

Who may benefit from the misinterpretations and misdirections of the study’s findings? We can take clues from the five applicable NIH grants (UL1-DE019580, RL1MH083268, RL1MH083269, RL1DA024853, PL1MH083271) and the researchers’ statement:

“We were able to predict choice category successfully in 71.8% of cases.”

Anybody ever read Philip K. Dick?

http://www.pnas.org/content/111/7/2470.full “Predicting risky choices from brain activity patterns”

We pay attention to the present through the windows of perception that we’ve developed from our past

My paraphrase of the 2013 study’s findings:

  • We pay attention to the present through the windows of perception that we’ve developed from our past;
  • The rest of the world is blocked by our consciousness’ perceptual thresholds.

It was good to read an attention study that didn’t zap the subjects’ brains.

http://www.pnas.org/content/111/4/E417.full “Prestimulus oscillatory power and connectivity patterns predispose conscious somatosensory perception”

Our long-term memory usually selects what we pay closer visual attention to

This 2014 human study at Vanderbilt found that our long-term memory usually selects what we pay closer visual attention to:

“Improvements in attentional tuning were accompanied by changes in an electrophysiological signal hypothesized to index long-term memory.”

The focus was on electrical fields, leading to predictable statements:

“Follow-up studies using neuroimaging techniques are needed to identify definitively the brain areas and associated networks responsible for the rapid changes in perceptual attention we observed.”

The researchers also found that 20 minutes of electrical brain stimulation helps tune perceptual attention. Is it in vogue that attention studies like this one and Can psychologists exclude the limbic system and adequately study awareness and social cognition? seemed to need gadgets that zapped the subjects’ brains?

http://www.pnas.org/content/112/2/625.full “Enhancing long-term memory with stimulation tunes visual attention in one trial”